11 Dec Alzhiemer disease
Alzhiemer disease
Alzheimer’s disease – Alzheimer’s disease is the most common form of dementia, making up roughly 70-75% of all dementia cases.Globally, over 55 million people live with dementia; Alzheimer’s constitutes the majority of it. Dementia is a general term for memory loss of and other cognitive abilities serious enough to interfere with our daily life. It is a neurodegenerative disease of the elderly mainly (over the age of 65 and above). Dementia is more prevalent among females (around 9.0%) than males (around 5.8%), as hormonal shift during menopause, genetic factors, X chromosome gene expression etc.. It imapcts the different age groups, although Alzhiemer is more common in elderly population, as aging brings various cellular changes, vascular and metabolic isues along with genetic predeposition, as Apolipoprotein E gene risk creating damage, accumulation of amyloid plaques and tau tangles, sedentary lifestyle etc.
This is generally characterized by brain tissue containing abundant amyloid plaques (deposits) surrounded by dead and dying neurons and neurofibrillary tangles (20-nm-diameter fibers). The amyloid plaques consist mainly of 40- to 42- residue peptide named amyloid-β peptide (Aβ). β-amyloid deposition is an ongoing process, at least in the later decades of life. This correlates with the age dependence of AD. However, early-onset AD is also reported and is considered to be inherited genetic disorder. Cholesterol transport protein apolipoprotein E (apoE) has been implicated in the premature onset of AD. The apoE gene has several normally occurring variants (alleles) like apoE2 (occurring in 15% of the population), apoE3 (78% occurrence), and apoE4 (7% occurrence). apoE4 is a major risk factor for the development as well as early onset of the Alzheimer’s. Neurofibrillary Tangles. Major steps as • Refolding or misfolding of β-amyloid protein endogenous to human brain tissue. • Senile plaques and neurofibrillary bundles contain aggregates of the protein βamyloid. • A 4.3-kDa polypeptide produced by proteolytic cleavage of a larger protein known as amyloid precursor protein. Levels of β-amyloid become elevated. • This protein undergoes a conformational transformation from a soluble α-helix to β-sheet and prone to self-aggregation. • Apolipoprotein E is a potential mediator of this conformational transformation.
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Other factors as Neurofibrillary tangles such as Tau protein becomes abnormal and forms tangles inside neurons; Neuroinflammation Overactivation of immune cells (microglia, astrocytes); Neurotransmitter Deficits especially acetylcholine, crucial for memory and learning; Modifiable Risk Factors Cardiovascular disease (hypertension, diabetes, obesity) Smoking, alcohol misuse,Physical inactivity, Poor diet, Social isolation,Traumatic brain injury,Chronic stress, depression.
Sustained inflammation contributes to neuronal injury.
Blocks transport of nutrients → neuronal degeneration. I t shows different symptoms at different stages as memory lapses, difficulty recalling recent events, sleep disturbances, loss of ability to communicate etc.
It can be diagnosed at various level as clinical evaluation with medical history, cognitive testing with MMSE, Neuropsychological testing, blood testing, CSF analysis etc, accordingly the treatment and medications provided with both Pharmacological and Non Pharmacological tratments.
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